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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Choroid plexus blood flow was measured in 29 adult female sheep using the radioactive microsphere technique. Basal blood flow, response to change in arterial carbon dioxide tension, and response to change in mean arterial blood pressure were determined. The results were compared to cerebral cortical blood flow values in the same sheep. Mean choroid plexus blood flow was 601 ml/100 g/min under basal conditions. Choroid plexus blood flow fell 31% with hypocarbia, a reduction comparable to that seen in cortex. With hypercarbia choroid plexus blood flow rose only 27% whereas cortical blood flow increased by 199%. Unlike cortical blood flow, choroid plexus blood flow fell significantly with pharmacogenic hypertension. The latter finding may reflect the absence of a blood-brain barrier in choroid plexus.
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PMID:Choroid plexus blood flow in the sheep. 677 16

Spinal cord tissue oxygen was measured by polarography at the dorsum of the spinal cord for 24 hours after acute spinal cord injury, and the effects of hypertension, hypercarbia, and hyperoxia were examined. Acute spinal cord injury was produced in mongrel dogs by constriction of the midthoracic cord with an epidural tourniquet inflated to 400 mm Hg, which was maintained for 5 minutes. At the injury site spinal cord tissue oxygen was slightly increased immediately after injury but was depressed significantly at 1 hour and remained unchanged thereafter. Hypertension induced by the intravenous infusion of norepinephrine elevated the tissue oxygen only slightly after 3 hours. Hypercarbia and hyperoxia produced by ventilation with a 95% O2:5% CO2 mixture did not elevate the depressed spinal cord oxygen content. When hypertension, hypercarbia, and hyperoxia were combined, the spinal cord oxygen value was elevated to the normal level even at 3 hours after injury, when the cord oxygen was at its lowest, and it increased steadily thereafter.
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PMID:Effects of hypertension and hypercarbia on spinal cord tissue oxygen in acute experimental spinal cord injury. 677 23

Combined hypertension and hypercarbia, which was found to improve post-traumatic spinal cord hypoxia and presumably ischemia in our previous study, was used in dogs subjected to experimental spinal cord injury to determine its therapeutic effects against acute spinal cord trauma. Intermittent hypertension and hypercarbia therapy, in which 15 minutes of hypertension and 95% O2:5% CO2 gas ventilation were alternated with 10 minutes of air ventilation, was given for 3 hours beginning 3 hours after injury. The treated dogs and untreated control dogs were checked neurologically and electrophysiologically at weekly intervals for up to 8 weeks. The treated dogs showed higher grades of neurological function within 1 week, but the results were statistically insignificant. Both groups demonstrated steady neurological improvement for the next 2 weeks and remained paraparetic thereafter with no group difference. The size of the intramedullary lesion was identical in both groups. Recovery of the somatosensory evoked potentials coincided well with neurological improvement, with again no difference between the two groups.
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PMID:Therapeutic trial of combined hypertension and hypercarbia on experimental acute spinal cord injury. 677 24

In this study, we compare the values of the systemic arterial pressure (S.A.P.), of the intracranial pressure (I.C.P.) and of the cerebral perfusion pressure (C.P.P.) -- (C.P.P. = P.A.S. -- I.C.P.) -- in the anesthetized dog, artificially ventilated, before and after vaporization with two halogenated anesthetics, enflurane and halothane at different concentrations. The measures were made in a group of ten dogs in normoventilation and intracranial normotension conditions, in one hypercapnic dog with intracranial hypertension, and in four dogs after injection of sodium laurylsulfate in the internal carotide to induce cerebral edema. In normocapnic dogs, enflurane and halothane increase the I.C.P., decrease the S.A.P. and the C.P.P. Under enflurane 0.5%, the I.C.P., the S.A.P., and the C.P.P. show no significant variations. The increase in I.C.P. is due to the cerebral vasodilator effect of the anesthetics. At equal concentrations, halothane is more hypotensive than enflurane, and the changes in C.P.P. induced by both anesthetics depend more on the variations in S.A.P. than on the variations in I.C.P. In the hypercapnic dog, the vaporization of enflurane and of halothane further enhance the increase in I.C.P., since the vasodilator effect of the anesthetics is added to that of hypercapnia. The S.A.P. and the C.P.P. drop in relation to the concentrations of vaporization used. After sodium laurylsulfate, the administration of enflurane and halothane is accompanied by a drop in S.A.P. and in C.P.P. In this group, the decrease in I.C.P. recorded in two thirds of the cases can be explained by the hypotensive effect of the anesthetics which decreased the hydrostatic pressure in the cerebral vascular bed, a maintenance element of the edema.
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PMID:Compared effects of enflurane and of halothane on the intracranial pressure and the cerebral perfusion pressure in the dog. 677 99

Cerebral air embolism can have hemodynamic effects such as increases in blood pressure and cerebral blood flow. It has been suggested that these factors play a role for the induction of the blood-brain barrier (BBB) dysfunction. In the present study, 5 microliters air was injected into the right internal carotid artery from a catheter in the external carotid artery after ligation of the extracerebral branches. No consistent change in blood pressure was observed with this small amount of air. Hypercapnia, which increases protein leakage in the brain under conditions of high intraluminal pressure, significantly reduced the extravasation in air embolism. Lidocaine and SITS (4 acetamido-4-isothiocyano-stilbene-2,2-disulfonic acid disodium), two drugs that effectively reduce the albumin leakage in acute hypertension, had no prophylactic effect in cerebral air embolism. Spontaneously hypertensive rats are less vulnerable than normotensive rats to pressure-induced BBB dysfunction but did not significantly differ from controls regarding albumin leakage in the present study. It is concluded that the increased cerebrovascular permeability in air embolism is not related to hemodynamic factors.
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PMID:Cerebral air embolism and the blood-brain barrier in the rat. 678 18

Ventilatory, airway occlusion pressure, arterial blood pressure and heart rate responses to isocapnic progressive hypoxia and to hypercapnia in high oxygen, both induced by a rebreathing method, were measured in 20 hypertensive male subjects aged 20 to 21 years with a diastolic blood pressure of 13.1 KPa +/- 0.34 SD (98 mmHg +/- 2.6 SD) and in 20 age-matched normotensive male subjects. Ventilatory, airway occlusion pressure and blood pressure response to hypoxia was significantly greater in the hypertensive subjects. Hypoxic ventilatory drive measured as the parameter A denoting the shape of the V1-O2 curve was 28.8 +/- 2.7 SEM (range 7.0 to 44.2) in the normotensive group and 116.1 +/- 10.5 SEM (range: 71.6 to 234.77) in the hypertensive group, the difference being highly significant (P less than 0.001). The magnitude of respiratory sinus arrhythmia (RSA) recorded during progressive hypoxia and plotted against either PA. O2 or VI values was significantly greater in the hypertensive group. The difference in ventilatory and circulatory responses to hyperoxic hypercapnia between the two groups of subjects was not significant. There was a significant correlation between the responses to hypoxia and hypercapnia in the normotensive subjects (r = 0.56, t = 2.861, P less than 0.01) but no correlation in the hypertensive subjects (r = 0.07). It is concluded that dissociation of the responsiveness of the peripheral and central chemosensitivity, the former being significantly increased and predominant, occurs in early, mild hypertension.
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PMID:Increased sensitivity of the arterial chemoreceptor drive in young men with mild hypertension. 680 56

1. Late cerebral arterial spasm was induced by repeated injections of autologous blood in a total amount of 14-33 ml into the basal cisterns of baboons to mimick subarachnoid hemorrhage (SAH). Regional cerebral blood flow (CBF), sagittal sinus pressure, cerebral arterial caliber from angiograms, and cerebral metabolic rate of oxygen (CMRO2) were measured before and after the experimental SAH to determine responses to hypercapnia and induced hypertension. The effect of the calcium antagonist, Nimodipine, on CBF autoregulation pre- and post-SAH was tested. 2. One week after the blood injections were started there was about 10-20% reduction, depending on territory measured, in the arterial diameter of the carotid and vertebral systems. This was associated with an 18% reduction in CBF and 9% decrease in the brain metabolism. 3. During hypercapnia before and after experimental SAH the flow increased with a mean of 3.7 and 1.8 ml, respectively, for each mm Hg elevation of PaCO2. In control animals, graded angiotensin-induced hypertension did not overtly affect CBF. Following SAH, the CBF autoregulation was impaired in 5 of 6 animals tested. 4. I.v. infusion of Nimodipine markedly curtailed the CBF autoregulation in pre-SAH animals and, to a somewhat slighter extent, also in post-SAH animals.
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PMID:Late cerebral arterial spasm: the cerebrovascular response to hypercapnia, induced hypertension and the effect of nimodipine on blood flow autoregulation in experimental subarachnoid hemorrhage in primates. 682 30

Systems analysis of the systemic arterial (SAPW), cerebrospinal fluid (CSFPW), and sagittal sinus (SSPW) pulse waves was carried out in 13 dogs during hypercapnia (5% CO2), intracranial normotension (inhalation of 100% O2), and intracranial hypertension (inhalation of 100% O2 plus an intraventricular infusion). Power amplitude and phase spectra were determined for each wave, and the power amplitude and phase transfer functions calculated between the cerebrospinal fluid (CSF) pressure and systemic arterial pressures, and between the sagittal sinus pressure and CSF pressure. The study indicates that the CSFPW and SSPW were virtually identical when impedance between the cerebral veins and sagittal sinus was minimal, which argues that the CSF pulse was derived from the cerebral venous bed. During inhalation of 100% O2, transmission of the SAPW across the precapillary resistance vessels into the cerebral venous pulse (as represented by the CSFPW) was nonlinear, while transmission across the lateral lacunae into the sagittal sinus was linear. During intracranial hypertension, wave transmission across the precapillary resistance vessels was linear, and across the lateral lacunae was nonlinear. During hypercapnia, wave transmission across the precapillary resistance vessels and the lateral lacunae was linear. When the wave transmission was nonlinear, there was also suppression in transmission of the lower harmonics, particularly the fundamental frequency, and a more positive phase transfer function, suggesting an inertial effect or decrease in acceleration of the pulse. Conversion from a nonlinear to linear transmission across the precapillary resistance vessels is evidence of loss of vasomotor tone, and is accompanied by rounding of the CSFPW. A vascular model which encompasses the above data and is based on flow in collapsible tubes and changes in vasomotor tone is posited to explain control of pulsatile flow and pulse waveform changes in the cerebrovascular bed. The model helps to clarify the strong interrelationship between intracranial pressure, cerebral blood flow, and cerebral autoregulation.
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PMID:Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation. 706 79

Hemodynamic monitoring was carried out in 9 newborn beagle puppies exposed to hypercarbic insult. 4 animals were exposed to slowly increasing carbon dioxide tensions without hypoxemia; 5 animals were exposed to rapid, intense increase in carbon dioxide tensions without hypoxemia. 2 of the 5 puppies (40%) exposed to the rapid hypercarbia developed intraventricular hemorrhage characteristic of that found in the immature human. All of the puppies exhibited germinal matrix layers comparable to those of 30- to 32-week gestational age human infants. Significantly higher systemic arterial and jugular venous pressures were documented during the baseline and experimental periods in the 2 animals that bled. A predisposition to hemorrhage may have been present in these 2 animals because of hypertension in the baseline period. This preliminary study demonstrates that a histological model for IVH exists in an animal which is stable enough for extensive hemodynamic monitoring.
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PMID:Intraventricular hemorrhage--an animal model. 718 62

This study summarizes our results with various ataralgesic combinations and their effects on circulation and respiration. Together with the new water-soluble 8-chloro-6-(2-fluorophenyl)-1-methyl-4H-imidazo[1,5-a][1,4]benzodiazepine midazolam, Ro 21-3981, Dormicum), 7-chloro-1,3-dihydro-1-methyl-5-phenyl-(2H)1,4-benzodiazepin-2-one (diazepam) and 5-(o-fluorophenyl)-1,3-dihydro-1-methyl-7-nitro-2H-1,4-benzodiazepin-2-one (flunitrazepam) are also considered, for the purpose of comparison. Pharmacokinetic studies confirm the clearly shorter duration of action of midazolam. The poor respiratory depressant action of the benzodiazepines can be easily and rapidly increased by premedication, ataralgesic combinations and substances for the prolongation of anaesthesia. Adequate spontaneous respiration is possible only in exceptional cases. The threshold doses for 100% suppression of cardiac stimulation due to 2-(o-chlorophenyl)-2-methylaminocyclohexanone (ketamine) were determined for all three benzodiazepines. These doses are also valid for hypertension. The effect of intubation is not suppressed by the ataralgesic combination alone, whereas it does suppress the increase in pressure in the pulmonary circulation which is synchronous with the systemic blood pressure. The rise in intracranial pressure following ketamine alone is also prevented by premedication with benzodiazepines, which on the other hand offer no protection against certain other effects (hypoxia, hypercapnia, intubation), The same is true for increases in intraocular pressure. According to the results of investigations carried out, the new benzodiazepine midazolam justifies our hope for a substance with a similar basic effect, but with a clearly improved pharmacokinetic profile.
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PMID:[Cardiocirculatory and respiratory effects of the combination of midazolam and ketamine]. 719 33


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